Han Xiaoxu, Wang Xiuwen, Han Fangping, Yan Hongxia, Sun Jin, Zhang Xin, Moog Christiane, Zhang Conggang, Su Bin
Beijing Key Laboratory for HIV/AIDS Research, Clinical and Research Center for Infectious Diseases, Beijing Youan Hospital, Capital Medical University, Beijing, 100069, China.
Sino-French Joint Laboratory for HIV/AIDS Research, Sino-French Joint Laboratory for Research on Humoral Immune Response to HIV Infection, Beijing Youan Hospital, Capital Medical University, Beijing, 100069, China.
Infection. 2025 Apr;53(2):495-511. doi: 10.1007/s15010-024-02429-0. Epub 2024 Nov 7.
Mycobacterium tuberculosis (M. tuberculosis) infection is the most common opportunistic infection in human immunodeficiency virus-1 (HIV-1)-infected individuals, and the mutual reinforcement of these two pathogens may accelerate disease progression and lead to rapid mortality. Therefore, HIV-1/M. tuberculosis coinfection is one of the major global public health concerns. HIV-1 infection is the greatest risk factor for M. tuberculosis infection and increases the likelihood of endogenous relapse and exogenous reinfection with M. tuberculosis. Moreover, M. tuberculosis further increases HIV-1 replication and the occurrence of chronic immune activation, accelerating the progression of HIV-1 disease. Exploring the pathogenesis of HIV-1/M. tuberculosis coinfections is essential for the development of novel treatments to reduce the global burden of tuberculosis. Innate immunity, which is the first line of host immune defense, plays a critical role in resisting HIV-1 and M. tuberculosis infections. The role of the cyclic guanosine monophosphate-adenosine monophosphate synthase (cGAS)-stimulator of interferon genes (STING) signaling pathway, which is a major DNA-sensing innate immune signaling pathway, in HIV-1 infection and M. tuberculosis infection has been intensively studied. This paper reviews the role of the cGAS-STING signaling pathway in HIV-1 infection and M. tuberculosis infection and discusses the possible role of this pathway in HIV-1/M. tuberculosis coinfection to provide new insight into the pathogenesis of HIV-1/M. tuberculosis coinfection and the development of novel therapeutic strategies.
结核分枝杆菌（M. tuberculosis）感染是人类免疫缺陷病毒1型（HIV-1）感染者中最常见的机会性感染，这两种病原体的相互作用可能会加速疾病进展并导致快速死亡。因此，HIV-1/M. tuberculosis合并感染是全球主要的公共卫生问题之一。HIV-1感染是M. tuberculosis感染的最大风险因素，会增加M. tuberculosis内源性复发和外源性再感染的可能性。此外，M. tuberculosis会进一步增加HIV-1复制以及慢性免疫激活的发生，加速HIV-1疾病的进展。探索HIV-1/M. tuberculosis合并感染的发病机制对于开发新的治疗方法以减轻全球结核病负担至关重要。固有免疫作为宿主免疫防御的第一道防线，在抵抗HIV-1和M. tuberculosis感染中起关键作用。环磷酸鸟苷-磷酸腺苷合成酶（cGAS）-干扰素基因刺激因子（STING）信号通路作为主要的DNA感应固有免疫信号通路，在HIV-1感染和M. tuberculosis感染中的作用已得到深入研究。本文综述了cGAS-STING信号通路在HIV-1感染和M. tuberculosis感染中的作用，并讨论了该通路在HIV-1/M. tuberculosis合并感染中的可能作用，以期为HIV-1/M. tuberculosis合并感染的发病机制及新治疗策略的开发提供新的见解。
